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  • Title: A functional promoter polymorphism in NFKB1 increases susceptibility to endometriosis.
    Author: Zhou B, Rao L, Peng Y, Wang Y, Qie M, Zhang Z, Song Y, Zhang L.
    Journal: DNA Cell Biol; 2010 May; 29(5):235-9. PubMed ID: 20218898.
    Abstract:
    Numerous proinflammatory cytokines, such as TNFalpha and IL-6, which are nuclear factor kappaB (NF-kappaB) target genes, have been shown to promote proliferation in endometriotic cells, and several other genes involved in promoting growth are also NF-kappaB target genes. The aim of this study was to investigate whether the functional insertion/deletion polymorphism (-94 insertion/deletion ATTG) in the promoter of nuclear factor kappaB gene (NFKB1) is associated with susceptibility to endometriosis. Polymerase chain reaction-polyacrylamide gel electrophoresis method was used to genotype the NFKB1 -94 insertion/deletion ATTG polymorphism in 206 women with endometriosis and 365 ethnicity-matched healthy control women. The genotyping method was confirmed by the DNA sequencing analysis. Genotype at the -94 insertion/deletion ATTG polymorphism in the NFKB1 promoter was in Hardy-Weinberg equilibrium in either case or control subjects. The frequency of the ATTG(2)/ATTG(2) genotype and ATTG(2) allele in the endometriosis was significantly higher than that of control subjects (59.7% vs. 37%, odds ratio = 3.069, p < 0.001 for ATTG(2)/ATTG(2) genotype; 75.2% vs. 59.7%, odds ratio = 2.049, p < 0.001 for ATTG(2) allele), indicating that the -94 insertion/deletion ATTG polymorphism in the NFKB1 promoter was associated with endometriosis. This study suggests that the functional -94 insertion/deletion ATTG polymorphism in the promoter of NFKB1 is associated with an increased risk for endometriosis.
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